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G protein‐activated inwardly rectifying K + (GIRK) currents in dendrites of rat neocortical pyramidal cells
Author(s) -
Takigawa Tomoko,
Alzheimer Christian
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.0385t.x
Subject(s) - g protein coupled inwardly rectifying potassium channel , biophysics , neuroscience , chemistry , patch clamp , dendrite (mathematics) , hyperpolarization (physics) , g protein , electrophysiology , biology , receptor , biochemistry , stereochemistry , geometry , mathematics , nuclear magnetic resonance spectroscopy
1 We performed patch‐clamp recordings on acutely isolated dendritic segments and cell somata of rat neocortical pyramidal neurons to determine and compare the relative density of G protein‐activated K + (GIRK) currents in the two cellular compartments. 2 Hyperpolarizing voltage ramps and elevation of extracellular K + concentration to 40 mM served to identify inwardly rectifying K + currents. Near‐saturating concentrations of adenosine (100 μ m ), baclofen (20 μ m ) and serotonin (20 μ m ) all produced robust GIRK currents in cell somata as well as in dendritic segments that were completely abolished by Ba 2+ (200 μ m ). In addition to agonist‐activated GIRK currents, both somata and dendrites displayed a constitutive Ba 2+ ‐sensitive inward rectification. 3 In order to compare the relative strengths of GIRK current responses in the two compartments, GIRK conductance was normalized to surface area. In contrast to intrinsic, G protein‐independent inward rectification, which was comparable in size in the two compartments, all three agonists evoked significantly larger GIRK conductances in dendrites than in somata. 4 Our data suggest that several neurotransmitters might employ GIRK currents as a tool to directly modulate the electrical properties of dendrites. In concert with voltage‐dependent K + currents and the hyperpolarization‐activated cation current ( I h ) of the dendrite, GIRK currents should dampen dendritic excitability and thus influence various aspects of dendritic signal integration.